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Pharmacology > Immunology and Inflammation > Flashcards

Immunology and Inflammation Flashcards

1
Q

What cells are activated during an innate immune response?

A

‘First response’

Granulocytes (bac-neutrophils, parasites-eiosinophils, basophils)
Mast cells
APCs

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2
Q

What two types of cells are commonly APCs?

A

Macrophages

Dendritic cells

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3
Q

How do APCs come to have antigens to be presented?

A

Phagocytose bacterium and parasites, through digestion antigens are produced and displayed on cell surface

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4
Q

CD4+ cells are also known as _______ and more specific to _______.

A

T helper cells
bacteria

(displayed along with MHC II protein)

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5
Q

CD8+ cells are also known as _______ and more specific to _______.

A

Cytotoxic T cells (nucleated)
viruses

(displayed along with MHC I protein, like all other nucleated cells in the body)

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6
Q

Activation of the adaptive immune system means involvement of what two cells?

A

T and B cells

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7
Q

What does humoral immunity involve?

A

Activation of B cells and Ab’s

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8
Q

What cells do cellular immunity involve and what do each do?

A

T helper cells (CD4+)- ‘effector cells’ regulate cytokines, B cells
Cytotoxic T cells ( CD8+)- mediates cell lysis/death

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9
Q

What two processes are Eicosanoids involved in?

A

Inflammation

Cellular signaling

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10
Q

What Eicosanoids arise from the lipooxygenase pathway?

A

Leukotrienes

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11
Q

What Eicosanoids arise from the cyclooxygenase pathway?

A

Prostaglandins
Prostacyclins
Thromboxanes

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12
Q

What is a common precursor to eicosanoids and via what two pathways can it be metabolized?

A

Arachidonic Acid

Lipooxygenase pathway and the Cyclooxygenase pathway

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13
Q

Explain how A.A. is broken down via the cyclooxygenase pathway.

A

A.A. is broken down by COX-1 and COX-2 which can lead to vasodilation, vasoconstriction, platelet inhibition and aggregation, fever, and bronchoconstriction

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14
Q

What are the two most common drugs used to inhibit the cyclooxygenase pathway?

A

NSAIDs

COX-2 inhibitors

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15
Q

What drugs can inhibit A.A. production and how?

A

Glucocorticoids (steroids) by inhibiting phospholipase A2, a precursor to A.A

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16
Q

Explain how A.A. is broken down via the lipooxygenase pathway.

A

A.A. is broken down by 5-lipooxygenase which can lead to:
Mast cells, basophils, and eosinophils (bronchoconstriction, vasoconstriction, dec. cor. blood flow, decrease cardiac contractility, etc)
OR
Neutrophils
(activation=migration, degranulation, eicosanoid synthesis, etc)

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17
Q

What drug can inhibit the 5-lipooxygenase, therefore inhibiting the lipooxygenase pathway?

A

Zileuton (FLAP inhbitors)

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18
Q

What is the pathophysiology of an allergic reaction?

A

An allergen stimulates the immune response. APCs engulf allergen and display on cells surface, activating T helper cells. T helpers cells recruit B cells to produce IgE specific to the allergen. IgE causes degranulation of mast cells and basophils which leads to the release of histamine and other inflammatory mediators

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19
Q

Local histamine vs systemic histamine release:

A

Local: erythema, edema, itching
Systemic: vasodilation, hypotension, bronchoconstriction

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20
Q

Where is histamine synthesized?

A

Mast cells and basophils (Inflam mediator)
Gastric mucosal cells (Regulates gastric acid secretion)
Neurons in the CNS (Regulates neurotransmission)

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21
Q

Where are H1 receptors found?

A

Smooth muscle, vascular endothelium, brain

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22
Q 
What is H1's effect on: 
Lungs:
Vascular sm. muscle: 
Vascular endothelium: 
Peripheral nerves:
A

Lungs: bronchoconstriction (asthma)
Vasc. sm. muscle: postcapillary venule dilation (erythema)
Vasc. endothelium: cellular contraction (edema)
Peripheral nerves: sensitization (itching, pain)

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23
Q

Where are H2 receptors found?

A

Gastric parietal cells, cardiac muscles, mast cells, braine

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24
Q

What are H2’s effect on:
Heart:
Stomach:

A

Heart: minor increase in HR and contractility
Stomach: gastric acid secretion (PUD, GERD)

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25
Q

H1 antihistamines are inverse agonists because they ______________ .

A

Cause the H1 rc to be inactivated, stabilizing it.

H1 rc is in active state at baseline, H1 antihistamines cause the rc to be inactivated.

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26
Q

What type of rc are histamine rc’s?

A

seven-transmembrane G protein-coupled receptors

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27
Q

How are H1 antihistamines metabolized?

A

CYP 450

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28
Q

How well are H1 antihistamines absorbed and when do they reach their Cmax?

A

Very well absorbed.

Cmax 2-3hrs

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29
Q

Describe first generation H1 antihistamines:

A

Lipophilic
Neutral at physiologic pH
Easily cross BBB
Work faster

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30
Q

What are examples of first generation H1 antihistamines?

A 
Diphenhydramine 
Hydroxyzine
Chlorpheniramine
Promethazine 
Doxepin
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31
Q

Describe second generation H1 antihistamines:

A 
Highly albumin bound 
Ionized at physiologic pH
Does not cross BBB
Stay in pl. longer (dec. SE)
Hepatically metabolized
Work slower
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32
Q

What are examples of second generation H1 antihistamines?

A 
Loratidine 
Desloratidine 
Cetirizine 
Levocetirizine
Fexofenadine
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33
Q

What are H1 antihistamines most commonly used for?

A

Rhinitis, conjunctivitis, urticaria, pruritis

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34
Q

Are H1 antihistamines effective for systemic anaphylaxis or asthma?

A

No, antihistamines only affect histamine rc not local mediators.

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35
Q

First generation H1 antihistamines can also be used to treat:

A

Motion sickness, chemotherapy related n/v: diphenhydramine, dimenhydrinate, meclizine, promethazine

Insomnia: diphenhydramine, doxylamine (indicated for sleep)

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36
Q

How do diphenhydramine, dimenhydrinate, meclizine, and promethazine decrease motion sickness and chemo related n/v?

A

Inhibits histamine signals from the vestibular nucleus which is the control center for vomiting in the medulla

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37
Q

AE of H1 antihistamines include:

A 
Sedation 
Cardiac toxicity (QT prolongation, d/t CYP 3A4 interactions) 
Anticholinergic effects (pup. dilatation, dry eyes, dry mouth, urinary hesitancy)
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38
Q

How do sympathetic and parasympathetic tone affect the airway and at what receptors?

A

Sympathetic: Bronchodilation at the B2 rc
Parasympathetic: Bronchoconstriction at the muscarinic rc

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39
Q

The 3 main types of bronchodilators are:

A

B-agonists
Anticholinergics
Methylxanthines

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40
Q

Why are drugs such as terbutaline, albuterol, and levalbuterol more commonly used as bronchodilators in asthmatics?

A

They have more selectivity for B2 agonists. (sympathetic NS)

Epi for example is non selective and isoproterenol and metaproterenol affect B1 and B2 rc’s (could cause cardiac stim)

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41
Q

What is the onset, peak, and duration of action of B-agonists and how does that lend to their use?

A

Onset: 15-30mins
Peak: 30-60mins
Duration: 4-6 hrs

They are used as rescue inhalers and dose according to duration of action (poor ON control)

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42
Q

When would B-agonists be used prophylactically?

A

Prior to a known trigger (ex-exercise)

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43
Q

What are two commonly used LABA’s and what is their MOA?

A

Salmeterol and Formoterol

B2 agonists

44
Q

What is the duration of action of a LABA and why?

A

Duration: 12-24hrs

They contain lipophilic side chains that resist degradation making them long acting

45
Q

LABA’s should never be used as a __________, because they do not treat underlying ____________ .

A

monotherapy

inflammation

46
Q

LABA’s are good at prevention of:

A

bronchoconstriction

47
Q

How are salmeterol and formoterol different?

A

Salmeterol has a slower onset of action

48
Q

What is the black box warning associated with LABA’s?

A

They have been associated with asthma-related death and in pediatric and adolescent patients have increased the rate of hospitalizations

(do not dose alone, use with corticosteroid/short acting B2 agonist)

49
Q

What AE do LABA’s carry with them?

A

Cardiac toxicity risk

50
Q

How do anticholinergics work?

A

Competitive antagonists at muscarinic Ach rc (M3)

Prevent action of parasympathetic NS (bronchoconstriction)

51
Q

Three commonly used anticholinergics:

A
  1. Atropine
  2. Ipratropium bromide
  3. Tiotropium
52
Q

Why is atropine not typically used for the management of asthma?

A

It is highly absorbed across the resp. epithelium and causes systemic effects.
(tachycardia, nausea, dry mouth, GI upset)

53
Q

What is ipratropium bromide?

A

Anticholinergic agent
Ammonium salt derivative of atropine= charged molecules aren’t as systemically absorbed
Can causes local AE d/t deposition in mouth and oral absorption

Dosed 4-6hrs

54
Q

What is Tiotropium?

A

Anticholinergic agent
Similar to ipratropium but slower dissociation from rc = longer acting

Dosed daily

55
Q

What are anticholinergics most often used to treat?

A

COPD

Cholinergic stimulation is greater in COPD patients

56
Q

What are the 2 commonly used Methylxanthines?

A

Theophylline

Aminophylline

57
Q

What are the MOAs of Methylxanthines?

A

Inhibition of phosphodiesterase:
Airway smooth muscle-bronchodilation
Inflammatory cells- anti inflammatory

Secondary effects: Adenosine receptor antagonism:
Increased ventilation during hypoxia
Increased endurance of diaphragmatic muscles
Decreased mast cell release

58
Q

Why are Methylxanthines rarely used?

A

Narrow TI
Metabolized CYP 450 1A2
*cigarette smoking induced CYP 1A2
Arrhythmias and death can occur

59
Q

AE of Methylxanthines include:

A 
N/V/D 
HA
Irritability 
Insomnia 
Seizures 
Brain damage
Hypokalemia
Hypotension 
Cardiac arrhythmias
Death
60
Q

How can B agonists and Theophylline be used together?

A

B2 agonists will bind to G coupled receptor that causes the production of cAMP which increase activity of PKA leading to bronchodilation. Theophylline inhibits the breakdown of cAMP by inhibiting phosphodiesterase this leads to further bronchodilation

61
Q

What are the two main MOA of asthma?

A
  1. Bronchoconstriction d/t smooth muscle contraction

2. Inflammation

62
Q

What are AE of short acting B-agonists?

A

Tremors in hands

Tachycardia

63
Q

How are methylxanthines administered?

A

Orally

64
Q

How do corticosteroids aid in treatment of asthma and COPD?

A

Alter genetic transcription:

  • Increased B2 rc and anti-inflamm proteins
  • Decreases pro-inflamm protiens
  • Induces apoptosis in inflamm cells (eosinophils/T helper)
  • Indirect inhibition of mast cells
65
Q

Are corticosteroids a cure for asthma?

A

No, they are a suppressive treatment

66
Q

How are corticosteroids usually administered?

A

Inhaled.
25% reaches airway= higher conc. than when given PO.
Less systemic effects d/t CYP in GI tract and first pass
(if pts are on meds inhibiting first pass= increased systemic effects of corticosteroid)

67
Q

When are systemic corticosteroids administered?

A

Acute attacks

68
Q

What are AE of corticosteroids?

A 
Osteopenia/Osteoporosis
Delayed growth in children
Oropharyngeal candidiasis 
Hoarseness 
Hyperglycemia
69
Q

What are examples commonly used corticosteroids?

A

Beclomethasone
Triamcinolone
Fluticasone (avail in combo with salmeterol)
Budesonide (avail in combo with formoterol)
Flunisolide
Mometasone
Ciclesonide

70
Q

What is the MOA of Cromolyns?

A

Stabilize mast cells (inhibits release of inflamm mediators)

71
Q

What is the indication for use of a Cromolyn?

A

Prophylaxis.

Not effective after allergic response has been initiated

72
Q

What are the two Cromolyns and how often are they dosed?

A

Cromolyn and Nedocromil
4x/day
less systemic absorption than other inhalers

73
Q

What is Zileuton’s MOA?

A

Prevents 5-lipooxygenase from breaking down A.A. and producing leukotrienes
(Leukotriene inhibitor)

74
Q

What is the MOA of Motelukast and Zafirlukast?

A

Inhibits binding of leukotrienes to receptor in the airway

Leukotriene inhibitor

75
Q

All 3 Leukotriene inhibitors are hepatically metabolized, but which one has the greatest risk for hepatotoxicity?

A

Zileuton

76
Q

Leukotriene inhibitors have a ________ therapeutic index.

A

Wide

77
Q

What is the anti-IgE antibody agent and what is its MOA?

A

Omalizumab
(humanized mouse monoclonal Ab)
Binds to IgE, decreasing circulating IgE and prevents binding of IgE to mast cells.
It can cause the down regulation of receptors.

78
Q

How is Omalizumab administered, how often, and what is an AE?

A

subQ
q2-4wks
AE: (rare) triggering of immune response

79
Q 
Mild Intermittent Asthma: 
S/s = 2x/week 
Nocturnal awakenings =2x/month
Exacerbations brief
Lung function normal between exacerbations 
Limited peak flow variability

Short term and long term control

A

Short term: Short acting B-agonist PRN

Long term: None

80
Q

Mild Persistent Asthma:
S/s > 2x/week
Nocturnal awakenings > 2x/month
Exacerbations brief and may affect activity
Lung function normal when asymptomatic
Peak flow decreased 20-30% when symptomatic

Short term and long term control

A

Short term: Short-acting B agonist
Long term:
Preferred: Low dose inhaled corticosteroid
Alternative: Leukotriene pathway modifier, mast cell stabilizer, or theophyllin

81
Q 
Moderate Persistent Asthma: 
Daily s/s
Nocturnal awakenings >1x/week
Frequent exacerbations lasting days affecting activity
Lung function 60-80% predicted
Peak flow variability >30%

Short term and long term control

A

Short term: Short acting B agonist
Long term:
Preferred: Medium dose inhaled steroid and LABA
Alternatives: Medium dose inhaled steroid alone, low to medium dose inhaled steroid and sustained release theophylline, OR low to medium dose inhaled steroid and leukotriene pathway modifier

82
Q 
Sever Persistent Asthma: 
Continual s/s
Limited activity 
Frequent nocturnal awakenings 
Frequent, severe exacerbations 
Lung function <60% predicted 
Peak flow variability >30%

Short term and long term control

A

Short term: Short acting B agonist
Long term:
Preferred: High dose inhaled corticosteroid and LABA (oral corticosteroid if needed)

83
Q

Why are some asthmatics sensitive to ASA?

A

ASA inhibits the COX pathway which can cause shunting of A.A. to the other side of the pathway (lipooxygenase) causing leukotriene release, airway constriction, and edema= asthma attack

84
Q

Two most important questions to ask an asthmatic at an office visit?

A
  1. How often do you use your inhaler

2. How often do you wake up at night with s/s

85
Q

What type of drug might you start in the winter to prevent increased asthma symptoms in the spring d/t allergens?

A

Cromolyns

86
Q

What is hyperuricemia?

A

Abnormal levels of uric acid in the blood and urine

>7mg/dL

87
Q

What characterizes gout?

A
  • Hyperuricemia
  • Acute/chronic inflammatory response due to crystal formation in joints and tissues
  • Either a decrease in excretion or an increase in metabolic sythesis
88
Q

What causes primary gout?

A

Defect in purine metabolism and/or uric acid excretion

89
Q

What is secondary gout

A

D/t:
Cancer
CRF
Drugs- salicylates, antineoplastic drugs, diuretics, ethambutol, nicotinic acid, cyclosporine, ethanol

90
Q

What is the drug of choice for use in an acute gout attack?

A

NSAIDs (indomethicin)

can also use colchicine and prednisone/glucocorticoids

91
Q

Indications for use of Colchicine:

A 
Acute attack (rarely used now)
Prophylaxis in pts with chronic gout
92
Q

What is Colchine’s MOA?

A

Disruption of urate deposition and subsequent inflammatory reaction
*No effects of uric acid levels, works only on urate deposition

93
Q

AE of Colchicine:

A

Abdominal pain
n/v/D

Many drug interactions, cyclosporine, tacro, verapamil

94
Q

What are the two drugs used for prophylaxis of gout?

A

Probenecid

Allopurinol

95
Q

Probenecid’s MOA:

A

Decrease urate reabsorption in the proximal tubules increasing elimination
Non-selective blockade of active renal transport of organic acids

96
Q

What does probenecid’s non-selective blockade run the risk of?

A

DI, can block secretion of drugs and increase levels (pcn, naproxen)

97
Q

AE of Probenecid:

A

Hypersensitivity

GI distress

98
Q

When should you not use probenecid and why?

A

During an acute attack because it could lead to kidney stones

99
Q

Precautions when starting probenecid include:

A

Increase in frequency, duration, and severity of attacks could occur during first 6-12months
To maintain fluid intake of >2L/day
Give bicarb if needed

100
Q

What is the MOA of Allopurinol?

A

Inhibits uric acid production by inhibiting xanthine oxidase
Allopurinol is a prodrug that is converted to its active form by xanthine oxidase

101
Q

If acute attack occurs d/t disruption in urate equilibrium d/t allopurinol administration, what can be administered?

A

Colchicine

102
Q

When administering azathioprine with allopurinol the dose of azathioprine should be significantly ________ .

A

Decreased

103
Q

Abrupt cessation of corticosteroids could lead to:

A

Addisonian crisis

104
Q

Inhaled corticosteroids are given at lower doses because they avoid:

A

First pass metabolism

105
Q

Which anti-gout medication is excreted in the urine and the bile and therefore has many drug interactions?

A

Colchicine

Pharmacology (48 decks)

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